Bexton R S, Hellestrand K J, Nathan A W, Spurrell R A, Camm A J
Eur Heart J. 1983 Feb;4(2):92-102. doi: 10.1093/oxfordjournals.eurheartj.a061432.
Both the electrophysiological and antiarrhythmic effects of some antiarrhythmic agents may differ markedly depending on their route of administration. Flecainide acetate, a new class 1 agent, was therefore administered both intravenously and orally to 13 patients with recurrent paroxysmal tachycardia to assess whether the acute response to intravenous flecainide accurately predicts the response to oral therapy. Eight patients had atrioventricular re-entrant tachycardia (AVRT) and five patients intra AV nodal re-entrant tachycardia (AVNRT). When administered by either route, flecainide markedly prolonged both the anterograde and retrograde conduction intervals during constant rate pacing and the anterograde and retrograde Wenckebach cycle lengths during incremental pacing. Five of the 13 patients developed complete retrograde block after both routes of administration of the drug. All 13 patients received intravenous flecainide during tachycardia with successful reversion to sinus rhythm in all cases. Tachycardia could be reinitiated in five of the patients with AVRT after intravenous flecainide and in one further patient after oral administration. It was not possible to reinitiate tachycardia in any of the five patients with AVNRT after either intravenous or oral flecainide. The size of the tachycardia initiation windows, by either atrial or ventricular premature stimuli, were significantly reduced by both intravenous and oral flecainide. In those patients in whom tachycardia could be reinitiated, tachycardia cycle length was significantly increased, and to a similar degree, by both routes of administration of the drug. This increase in cycle length was predominantly due to prolongation in retrograde conduction. It is concluded that flecainide acetate is a potent antiarrhythmic agent for use in patients with junctional tachycardia. The intravenous administration of flecainide reliably predicts the subsequent response to oral therapy.
某些抗心律失常药物的电生理和抗心律失常作用可能因其给药途径的不同而有显著差异。因此,对13例复发性阵发性心动过速患者静脉内和口服给予新型I类药物醋酸氟卡尼,以评估静脉注射醋酸氟卡尼的急性反应是否能准确预测口服治疗的反应。8例患者患有房室折返性心动过速(AVRT),5例患者患有房室结内折返性心动过速(AVNRT)。无论通过哪种途径给药,氟卡尼在恒率起搏期间均显著延长前向和逆向传导间期,在递增起搏期间均显著延长前向和逆向文氏周期长度。13例患者中有5例在两种给药途径后均出现完全性逆向传导阻滞。所有13例患者在心动过速期间均接受了静脉注射氟卡尼,所有病例均成功转为窦性心律。静脉注射氟卡尼后,5例AVRT患者中有1例在口服给药后可再次诱发心动过速。静脉或口服氟卡尼后,5例AVNRT患者均无法再次诱发心动过速。静脉和口服氟卡尼均显著减小了由房性或室性早搏刺激引起的心动过速诱发窗口的大小。在那些可以再次诱发心动过速的患者中,两种给药途径均使心动过速周期长度显著增加,且增加程度相似。这种周期长度的增加主要是由于逆向传导的延长。结论是醋酸氟卡尼是一种用于交界性心动过速患者的有效抗心律失常药物。静脉注射氟卡尼可可靠地预测随后口服治疗的反应。